Zinc oxide nanoparticles (ZnO NPs) generate reactive oxygen species and thus induce phototoxicity against bacteria and cancer cells due to their photocatalytic effects under light irradiation. This review introduces and discusses recent research regarding the utilization of ZnO NPs for light-triggered antibacterial and anticancer activities.

Polysorbates (PSs) are synthetic nonionic surfactants consisting of polyethoxy sorbitan fatty acid esters. PSs have been widely employed as emulsifiers and stabilizers in various drug formulations and food additives. Recently, various PS-based formulations have been developed for safe and efficient drug delivery. This review introduces the general features of PSs and PS-based drug carriers, summarizes recent progress in the development of PS-based drug formulations, and discusses the physicochemical properties, biological safety, P-glycoprotein inhibitory properties, and therapeutic applications of PS-based drug formulations. Additionally, recent advances in brain-targeted drug delivery using PS-based drug formulations have been highlighted. This review will help researchers understand the potential of PSs as effective drug formulation agents.

The Warburg effect is important for cancer cell proliferation. This phenomenon can be flexible by interaction between glycolysis and mitochondrial oxidation for energy production. We aimed to investigate the anticancer effects of the pyruvate dehydrogenase kinase inhibitor, dichloroacetate (DCA) and the mitochondrial respiratory complex I inhibitor metformin in liver cancer cells. The anticancer effect of DCA and/or metformin on HepG2, PLC/PRF5 human liver cancer cell lines, MH-134 murine hepatoma cell lines, and primary normal hepatocytes using MTT assay. Inhibition of lactate/ATP production and intracellular reactive oxygen species generation by DCA and metformin was investigated. Inhibition of PI3K/Akt/mTOR complex I was evaluated to see whether it occurred through AMPK signaling. Anticancer effects of a combination treatment of DCA and metformin were evaluated in HCC murine model. The results showed that metformin and DCA effectively induced apoptosis in liver cancer cells. A combination treatment of metformin and DCA did not affect viability of primary normal hepatocytes. Metformin upregulated glycolysis in liver cancer cells, thereby increasing sensitivity to the DCA treatment. Metformin and DCA inhibited mTOR complex I signaling through upregulated AMPK-independent REDD1. In addition, metformin and DCA increased reactive oxygen species levels in liver cancer cells, which induced apoptosis. A combination treatment of metformin and DCA significantly suppressed the tumor growth of liver cancer cells using in vivo xenograft model. Taken together, the combined treatment of metformin and DCA suppressed the growth of liver cancer cells. This strategy may be effective for patients with advanced liver cancer.